Dietary polyunsaturated fatty acids (PUFA) play a major role in the regulation of immune responses during infection and inflammation. Linoleic acid (LA:18:2.omega.6) is the precursor for the formation of arachidonic acid which is metabolized to proinflammatory mediators such as prostaglandins (PG)E.sub.2 and thromboxane (Tx)A.sub.2. Other polyunsaturated fatty acids such as .alpha.-linolenic acid (18:3.omega.6) and .gamma.linolenic acid (18:3.omega.6) are precursors for the formation of eicosapentaenoic acid (EPA: 20:5.omega.3) and dihomo-.gamma.-linolenic acid (DGLA: 20:3.omega.6), respectively, both of which displace arachidonic acid (20:4.omega.6), reduce the production of PGE.sub.2 and also form mediators such as PGE.sub.3 and PGE.sub.1 which are less inflammatory. Thus, dietary fats rich in .gamma.-linolenic acid, .alpha.-linolenic acid, or EPA have been employed to modulate some of the inflammatory responses in experimental animal models (Carrick et al., Shock 2:421-426 (1994); Yacoob and Calder, Cell Immunol 163:120-128 (1995)) and in clinical trials (Espersen et al., Clin Rheumatol ll:393-395 (1992); Engler et al., J Hyperien 10(1):197-204 (1992); Harrobin, Rev Contem Pharmacol. Ther. 1:1-45 (1990)).
Recently, it has been demonstrated that in animals fed sesame seed oil (SSO), an increased survival in mice exposed to a lethal dose of LPS is associated with a substantial increase in the accumulation of dihomo-.gamma.-linolenic acid (Chavali et al., Int Arch Allergy Immunol 114:153-160 (1997)). Moreover, the experimental data suggest that these beneficial effects are attributed to the lignans in the non-fat portion of the oil. These lignans, including sesamin, episesamin, sesaminol and sesamolin but not sesamol, inhibit the activity of .DELTA.-5 desaturase enzyme in vitro (Shimizu et al., Lipids 26:512-516 (1991)). Unlike sesamol (3,4-methylenedioxyphenol), the other lignans are dimeric compounds and have in common a methylene-bridged 3,4-dihydroxyphenol moiety (FIGS. 1A and 1B). Further, data (Shimizu et al., Lipids 26:512-516 (1991); Fujiyama et al., J Nutr Sci Vitaminol 41:217-225 (1995)) suggest that sesamin inhibits the .DELTA.-5 desaturase activity of .omega.6 polyunsaturated fatty acids, resulting in an accumulation of dihomo-.gamma.-linolenic acid. In mice fed sesamin, the LPS-induced production of PGE.sub.2, IL-10 and IL-6 was lower and that of TNF-.alpha. was higher, while these levels are unaffected in SSO fed animals (Chavali et al., Int Arch Allergy Immunol 114:153-160 (1997)).